Selective losses of brainstem catecholamine neurons after hypoxia-ischemia in the immature rat pup.

Abstract:

:Hypoxic-ischemic (HI) injury in the preterm neonate incurs numerous functional deficits, however little is known about the neurochemically-defined brain nuclei that may underpin them. Key candidates are the brainstem catecholamine neurons. Using an immature animal model, the postnatal day (P)-3 (P3) rat pup, we investigated the effects of HI on brainstem catecholamine neurons in the locus coeruleus, nucleus tractus solitarius (NTS), and ventrolateral medulla (VLM). On P21, we found that prior P3 HI significantly reduced numbers of catecholaminergic neurons in the locus coeruleus, NTS, and VLM. Only locus coeruleus A6, NTS A2, and VLM A1 noradrenergic neurons, but not NTS C2 and VLM C1 adrenergic neurons, were lost. There was also an associated reduction in dopamine-beta-hydroxylase-positive immunolabeling in the forebrain. These findings suggest neonatal HI can affect specific neurochemically-defined neuronal populations in the brainstem and that noradrenergic neurons are particularly vulnerable to HI injury.

journal_name

Pediatr Res

journal_title

Pediatric research

authors

Buller KM,Wixey JA,Pathipati P,Carty M,Colditz PB,Williams CE,Scheepens A

doi

10.1203/PDR.0b013e3181659774

subject

Has Abstract

pub_date

2008-04-01 00:00:00

pages

364-9

issue

4

eissn

0031-3998

issn

1530-0447

pii

00006450-200804000-00006

journal_volume

63

pub_type

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